Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe最新文献

{"title":"Catechin ameliorates hepatocellular damage caused by coadministration of isoniazid and rifampicin","authors":"Sonam Sahu ,&nbsp;Nimisha Paul ,&nbsp;Ankit Ganeshpurkar ,&nbsp;Nazneen Dubey ,&nbsp;Aditya Ganeshpurkar","doi":"10.1016/j.arres.2024.100107","DOIUrl":"10.1016/j.arres.2024.100107","url":null,"abstract":"<div><p>It is well known that phyto-constituents possess hepatoprotective properties. The radical scavenging potential of catechin has received substantial research. The goal of the current study was to assess the beneficial effect of Catechin to safeguard rats from liver damage caused by isoniazid and rifampicin. In this investigation, Wistar rats were employed. Administration of isoniazid (100 mg/kg) with rifampicin (100 mg/kg) for 21 days caused hepatocellular injury. The dosages of catechin used were 25, 50, and 100 mg/kg body weight. Blood was drawn at the end of the study, and biochemical tests were performed to determine the enzyme levels. Restoration of AST, ALT, and ALP was brought about by catechin administration (25, 50, and 100 mg/kg body weight). The administration lead to in a restoration of the SOD and catalase levels. The expression of TNF-α, IL-1β, IL-6, MDA, and nitric oxide decreased. The findings prove that catechin had a significant hepatoprotective impact. The hepatoprotective action of catechin might be mediated by the radical scavenging and cytokine suppressing effects.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"12 ","pages":"Article 100107"},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137924000146/pdfft?md5=ed1de63fa0ac231b837c894e6379cd38&pid=1-s2.0-S2667137924000146-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141710775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidative stress in patients with congenital heart disease: A systematic review","authors":"Inne Vanreusel ,&nbsp;Jan Taeymans ,&nbsp;Emeline Van Craenenbroeck ,&nbsp;Vincent F.M. Segers ,&nbsp;An Van Berendoncks ,&nbsp;Jacob J. Briedé ,&nbsp;Wendy Hens","doi":"10.1016/j.arres.2024.100109","DOIUrl":"10.1016/j.arres.2024.100109","url":null,"abstract":"<div><p>Congenital heart disease (CHD) represents a prevalent and diverse set of clinical conditions with significant morbidity and mortality. A recent meta-analysis indicates elevated oxidative stress levels in CHD patients compared to healthy controls. This review aims to elucidate the precise role of oxidative stress and its contributors in CHD. A systematic search of English-language publications on PubMed and the TRIP database yielded 29 reports analyzing oxidative stress markers in peripheral blood samples from pediatric and adult CHD populations. Only studies comparing oxidative stress markers either against controls, within CHD groups, or assessing oxidative stress markers over time evaluating the effect of an antioxidant treatment were included, followed by bias risk assessment. The different markers assessing oxidative stress in CHD were summarized, with scrutiny on potential influencing factors. Although findings are inconclusive overall, factors like cyanosis, genetic predispositions, and metabolic status emerge as important contributors. Additionally, multiple studies suggest a correlation between oxidative stress and CHD severity. Notably, no antioxidant therapies have been evaluated for reducing oxidative stress in CHD patients to date. Further research is imperative for a comprehensive understanding of CHD pathophysiology, particularly the heightened vulnerability of the right ventricle (RV) to heart failure (HF). Such insights could facilitate the development of tailored therapies for RV-related HF and dedicated antioxidant treatments, crucial for enhancing survival rates in this patient population.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"12 ","pages":"Article 100109"},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266713792400016X/pdfft?md5=b5750b174f3e01dd37d713fb7bf5aee3&pid=1-s2.0-S266713792400016X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141840481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oral administration of glutathione modulates exercise-related metabolic and oxidative factors in skeletal muscles of mice","authors":"Wataru Aoi ,&nbsp;Kenji Sato","doi":"10.1016/j.arres.2024.100104","DOIUrl":"https://doi.org/10.1016/j.arres.2024.100104","url":null,"abstract":"<div><p>Exercise activates the metabolic system in skeletal muscles, which is modulated by antioxidant supplementation. Some antioxidants such as glutathione accelerate metabolic adaptation induced by exercise training, whereas other antioxidants such as vitamin C suppress it. Thus, the present study aimed to elucidate the effects of oral administration of glutathione and vitamin C on metabolic and redox responses after acute exercise in mice. ICR mice were randomly divided into sedentary, exercise, exercise with glutathione, and exercise with vitamin C groups. In the exercise groups, mice were subjected to treadmill running at 30 m/min for 30 min. Immediately after exercise, glutathione (2% w/v, 5uL/g body weight) or vitamin C (10% w/v, 5uL/g body weight) were administered. Gastrocnemius muscle and plasma samples were collected at 3 h post-exercise. We found that plasma creatine kinase levels were only elevated in the exercise group. Malondialdehyde levels in skeletal muscle were elevated after exercise, but this elevation was suppressed by glutathione administration. PGC-1α expression was increased in both the exercise and glutathione groups compared with the sedentary group; however, the expressions of its downstream proteins were only increased in the glutathione group. Reduced glutathione form was notably increased in the mitochondria, whereas oxidized glutathione was significantly increased in the cytosol of the glutathione administration group compared with the exercise group. Thioredoxin reductase activity was also higher in the glutathione group than in the sedentary and exercise groups. Thus, this study demonstrates that post-exercise glutathione administration accelerates the exercise-induced responses of mitochondrial factors in skeletal muscle, which may be mediated by the modulation of the redox system.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"12 ","pages":"Article 100104"},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137924000110/pdfft?md5=4b75fb741b9f4f2a6527ae9eaa5923e1&pid=1-s2.0-S2667137924000110-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141240370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biological uses of nanomaterials within the safe handling and toxic effects: (Brain as a model)","authors":"Essia Hamdi,&nbsp;Slah Hidouri","doi":"10.1016/j.arres.2024.100105","DOIUrl":"https://doi.org/10.1016/j.arres.2024.100105","url":null,"abstract":"<div><p>Living organisms are prone to different types of nanomaterials and the interaction leads to biochemical alteration depending on the dose of received nanomaterials. At an average dose, nanoparticles cause toxicity, and they may induce oxidative stress by shifting the oxidoreduction equilibrium. Using a relatively low dose, nanoparticles can be beneficial in nanomedicine to correct deficiencies of essential elements. Moreover, nanoparticles can serve as carriers to deliver entrapped drugs through complex physiological media and finally reach the target organs or cells and release the drugs. Living cells have developed various strategies to nullify the effects of nanoparticles beyond their normal amount and release the key components retained by these particles. This review is focused on the nanoparticles' effects screening and investigates the correction of the nanotoxicity by the reported protective agents to make the use of nanoparticles safer. The model of this study concerns the brain as a highly sensitive organ and well protected by the blood barrier.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"12 ","pages":"Article 100105"},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137924000122/pdfft?md5=d16c64f7df231a1c226e674b96d1f880&pid=1-s2.0-S2667137924000122-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141540668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti- and pro-oxidant properties of polyphenols and their role in modulating glutathione synthesis, activity and cellular redox potential: Potential synergies for disease management","authors":"Courage Sedem Dzah ,&nbsp;Haihui Zhang ,&nbsp;Vera Gobe ,&nbsp;David Asante-Donyinah ,&nbsp;Yuqing Duan","doi":"10.1016/j.arres.2024.100099","DOIUrl":"https://doi.org/10.1016/j.arres.2024.100099","url":null,"abstract":"<div><p>Cellular metabolic activities are controlled by pathways catalyzed by enzymes, closely regulated by signal transduction through induction or inhibition processes. Metabolic disorders and cellular dysregulation are often linked to redox-dependent signaling in a complex relationship. Glutathione (GSH) and polyphenols which are known regulators of cellular redox homeostasis have been studied immensely. However, no study has considered their potential interactions and synergies as novel mechanisms to control cellular disorders. GSH does not only act as an antioxidant, but as a ligand that binds to inactivate enzymes and toxins. Also, depending on cellular environment, structure, pH, concentration and availability of transition metals of high charge density, polyphenols may possess either anti-oxidant or pro-oxidant properties. Owing to their remarkable influence on cellular redox potential and metabolic signaling as individual compounds, this study considered the potential interactions and synergies between GSH and polyphenols in disease management. Generally, both GSH and polyphenols reduce oxidative stress in normal cells and may under exacerbating conditions of low GSH/GSSG ratio, induce apoptotic mechanisms in abnormal cells. Investigating the effects of pH, polyphenol and GSH concentrations, availability of transition metals, caloric restriction and polyphenol structure on apoptosis and proliferation in cancer cells in the future may be a basis for the synergistic exploitation of GSH and polyphenols in disease management.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"11 ","pages":"Article 100099"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137924000067/pdfft?md5=6ad9a6d88ddbb84d976fa5ac5e78713d&pid=1-s2.0-S2667137924000067-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140551205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ameliorative role of melatonin against adrenaline induced oxidative stress mediated cardiac and hepatic tissue injuries through preserving pyridoxine metabolism in male Wistar rats: A mechanistic insight","authors":"Manisha Mukhopadhyay ,&nbsp;Adrita Banerjee ,&nbsp;Romit Majumder ,&nbsp;Aindrila Chattopadhyay ,&nbsp;Debasish Bandyopadhyay","doi":"10.1016/j.arres.2024.100101","DOIUrl":"https://doi.org/10.1016/j.arres.2024.100101","url":null,"abstract":"<div><p>Adrenaline (AD) is a naturally occurring catecholamine, synthesised in the adrenal medulla to prepare the organisms for a \"fight or flight\" response. Under stressful circumstances, the circulatory catecholamine undergoes auto-oxidation, resulting in the formation of free radicals. Chronic stress results in the depletion of micronutrient stores in the body. Pyridoxine, often known as vitamin B₆, is an essential water-soluble vitamin that acts as a coenzyme in many metabolic processes. Therefore, our current investigation has prioritized the regulation of pyridoxine metabolism during the period of chronic stress and the precise role of melatonin, as a natural antioxidant, in preventing the alterations generated by adrenaline in cardiac and hepatic tissues. Adrenaline augmented the oxidative stress indices, leading to an imbalance in the antioxidative state resulting in changes in the levels of certain organ-specific serum markers, modifications in the levels of PL (pyridoxal), PLP (pyridoxal-5-phosphate), and the enzymes responsible for their metabolism and breakdown. The foregoing results were corroborated by the histochemical and histological examinations. Melatonin efficiently counteracted all these harmful changes. Besides, the current study demonstrates that both PLP and melatonin show efficacy in scavenging free radicals, including superoxide anion free radicals and hydroxyl radicals, in the chemical system. However, the in vitro studies demonstrated that when administered together, melatonin and PLP more effectively mitigate free radical generation than the individual molecule. These findings were further confirmed by the ITC binding study. These results suggest that a combination of melatonin and PLP could be a better therapeutic approach for the amelioration of stress induced oxidative damages in cardiac and hepatic tissues with an improved pyridoxine metabolism.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"11 ","pages":"Article 100101"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137924000080/pdfft?md5=5983a6daa91d4a63a5566e8650047ec3&pid=1-s2.0-S2667137924000080-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140605872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring miRNA function in maintaining redox mechanism of high altitude hypoxia associated maladies: An evidence based study","authors":"Richa Rathor,&nbsp;Geetha Suryakumar","doi":"10.1016/j.arres.2024.100103","DOIUrl":"https://doi.org/10.1016/j.arres.2024.100103","url":null,"abstract":"<div><p>The maintenance of balance between pro-oxidants and antioxidants is paramount for healthy aerobic cell status as cell may face oxidative stress if this balance is disturbed. During ascent to high altitude, reactive oxygen species (ROS) is enhanced and antioxidant system declined due to low oxygen availability. A number of evidences suggested the role of high altitude hypoxia in various maladies due to perturbed redox homeostasis. High altitude associated maladies include High Altitude Pulmonary Edema (HAPE), High Altitude Cerebral Edema (HACE), Acute mountain sickness (AMS), chronic mountain sickness (CMS), pulmonary hypertension, venous thrombosis, sleep disorders, muscle atrophy etc. Many supplementations such as vitamin C, vitamin E, resveratrol, β-carotene, quercetin, acetyl-l-carnitine, <em>Ginkgo biloba</em>, N-acetyl cysteine, selenium, <em>Ganoderma lucidum</em>, l-carnosine, ursolic acid have been extensively researched for counteracting the high altitude associated oxidative stress. However, most of the supplementations are having limited beneficial effects. However, miRNA can become an answer for high altitude associated pathophysiological conditions as miRNAs regulate energy metabolism, metabolic pathways, oxidative stress, inflammation etc. On that, miRNAs are easily assessable, highly specific and sensitive small molecules that can also exploited as a biomarker. To consider the seriousness of the problem, the present study screened out the miRNAs that are directly involved in maintaining NADPH oxidases (NOX), nitric oxide synthases (NOS), thioredoxin induced protein (TXNIP) and antioxidants enzymes, comprising superoxide dismutase (SOD), catalase, glutathione peroxidise (GPX), peroxiredoxins (PRDX), thioredoxins (TXN), thioredoxin reductase (TXNRD). After analysis with the screened miRNAs, the extraction of miRNA (12 miRNAs) was done that have role in regulating free radical producing enzymes such as NOS, NOX and TXNIP. It is hypothesized that regulating miRNAs could become a probable answer for high altitude associated maladies. Hence, further research in this direction is required to proof the concept.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"11 ","pages":"Article 100103"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137924000109/pdfft?md5=5c6a2ce0590a437f8a92f1cb77f87755&pid=1-s2.0-S2667137924000109-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140822678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal treatment with nitrite reduces pulmonary arteriolar remodeling in neonates with congenital diaphragmatic hernia","authors":"Alecsander F. Bressan ,&nbsp;Rebeca Lopes Figueira ,&nbsp;Karina Miura da Costa ,&nbsp;Antônio Landolffi Abdul Nour ,&nbsp;Graziela Cristina Ferreira ,&nbsp;Matheus V. Alavarse ,&nbsp;Rahul Gadde ,&nbsp;Alexandre Todorovic Fabro ,&nbsp;José Eduardo Tanus-Santos ,&nbsp;Lourenço Sbragia","doi":"10.1016/j.arres.2024.100102","DOIUrl":"https://doi.org/10.1016/j.arres.2024.100102","url":null,"abstract":"<div><p>Therapeutic use of alternative nitric oxide (NO) sources, such as nitrite and nitrate may be a protective influence on pulmonary vasculature abnormalities.</p></div><div><h3>Aim</h3><p>To evaluate whether the maternal administration of nitrite prevents the morphological and molecular changes that affect the pulmonary arterioles of congenital diaphragmatic hernia (CDH) neonates.</p></div><div><h3>Methods</h3><p>CEUA #88/2017. Sprague-Dawley neonate rats were divided into 6 groups: 1. control; 2. control + nitrite; 3. nitrofen exposed; 4. nitrofen exposed + nitrite; 5. CDH and 6. CDH + nitrite. The pregnant rats from nitrofen exposed and CDH groups were exposed to nitrofen on gestational day (GD) 9.5. The treatment with nitrite was made by gavage (15 mg/kg/day), on the last five gestational days. On GD 21.5 the fetuses were harvested. The following parameters were analyzed: lung and plasma nitrite concentration; media wall thickness (MWT) and endothelial NO synthase eNOS and inducible NO synthase iNOS immunohistochemistry of pulmonary arterioles.</p></div><div><h3>Results</h3><p>Nitrite treatment increased the maternal plasma concentration of nitrite in control and nitrofen-exposed rats. All neonates exposed to nitrofen showed an increase of nitrofen in the lung and plasma. Nitrite treatment decreased the MWT of pulmonary arterioles of CDH neonates. Nitrite treatment increased eNOS marker and attenuated iNOS marker in neonates with CDH.</p></div><div><h3>Conclusions</h3><p>Nitrite maternal treatment rescued the morphometry and recovered eNOS expression of CDH pulmonary arterioles during CDH. Nitrite is a potential prenatally therapeutic approach to vascular alterations present in CDH neonates.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"11 ","pages":"Article 100102"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137924000092/pdfft?md5=8e33401ba84a9fee00b5d8411968cb97&pid=1-s2.0-S2667137924000092-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140879998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The complex interplay between oxinflammation, mitochondrial dysfunction and lipotoxicity: Focus on their role in the pathogenesis of skeletal muscle insulin resistance and modulation by dietary fatty acids","authors":"Angelina Passaro ,&nbsp;Juana Maria Sanz ,&nbsp;Nenad Naumovski ,&nbsp;Domenico Sergi","doi":"10.1016/j.arres.2024.100100","DOIUrl":"https://doi.org/10.1016/j.arres.2024.100100","url":null,"abstract":"<div><p>Skeletal muscle insulin resistance is pivotal in the pathogenesis of type 2 diabetes mellitus (T2DM). Oxinflammation, referred to as the coexistence of and tight relationship between inflammation and oxidative stress, along with mitochondrial dysfunction and lipotoxicity have all been implicated in the pathogenesis of skeletal muscle insulin resistance. Most importantly, these effectors of insulin resistance are able to fuel one another, thereby generating a complex vicious cycle. This review aims at providing an updated and critical overview on the intimate cross-talk between oxinflammation, mitochondrial dysfunction and lipotoxicity as key molecular mechanisms underpinning insulin resistance. Additionally, the role of dietary fatty acids in modulating the key actors of this vicious cycle and the repercussions on skeletal muscle insulin sensitivity will be discussed in detail.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"11 ","pages":"Article 100100"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137924000079/pdfft?md5=e90d5091265f4aac902adf1c4677b64d&pid=1-s2.0-S2667137924000079-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140559002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recirculating bioavailable nicotine metabolite using ascorbic acid: A pragmatic approach for treating nicotine dependence","authors":"Murugesan Arumugam ,&nbsp;Raman Lakshmi Sundaram ,&nbsp;Vishal Jayajothi ,&nbsp;Manish Arul ,&nbsp;Jerad A Suresh ,&nbsp;Sathesh Kumar Kesavan","doi":"10.1016/j.arres.2023.100089","DOIUrl":"https://doi.org/10.1016/j.arres.2023.100089","url":null,"abstract":"<div><p>Nicotine undergoes metabolism, converting into the oxidized metabolite cotinine, which can persist in the body for several weeks and potentially lead to fatal conditions, such as cancer. Conventional nicotine replacement therapy provides additional nicotine to the body, thereby increasing the chance of accumulating the toxic metabolite cotinine. Consequently, we proposed a hypothesis: converting cotinine back into nicotine using a suitable reducing agent, such as ascorbic acid, could be a practical approach. This conversion would allow cotinine to be reutilized for its central nervous system effects before its eventual elimination from the body. In the current study, we examined this hypothesis by using plasma samples from smokers. Volunteers (both non-smokers and smokers) were screened and recruited for this study. In the initial time- and dose-dependent studies, we incubated plasma samples from non-smokers with cotinine and ascorbic acid. Changes in cotinine and nicotine levels were quantified using HPLC-PDA. Based on the findings of these experiments, we selected a concentration of 1 µM ascorbic acid and incubated it with plasma samples from 25 smokers for 10 min. A time-dependent study revealed that nicotine was detected in non-smokers' plasma samples after a 10-minute incubation with 28.38 µM of both cotinine and ascorbic acid. In a subsequent dose-dependent study, the maximum concentration of nicotine was observed at 1 µM ascorbic acid. Among the 25 samples of smokers’ plasma, the mean nicotine concentration increased from 0.565 ± 0.196 to 1.937 ± 0.622 µM (<em>P</em> = 0.0081), while cotinine levels decreased from 1.278 ± 0.253 to 0.754 ± 0.137 µM (<em>P</em> = 0.0087). This study conclusively demonstrated that ascorbic acid, at a specified concentration, effectively converts cotinine back into nicotine in smokers' plasma. Importantly, this conversion did not occur in water or in the absence of ascorbic acid in the plasma, indicating enzyme involvement.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"10 ","pages":"Article 100089"},"PeriodicalIF":0.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137923000292/pdfft?md5=8cd5c7ca0e9e1be41972c27b4d8ccf6e&pid=1-s2.0-S2667137923000292-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138490208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}